Please use this identifier to cite or link to this item: http://hdl.handle.net/11452/30518
Title: Epigallocatechin-3-gallate reduces the proliferation of benign prostatic hyperplasia cells via regulation of focal adhesions
Authors: Soya, Elif
Korkmaz, Mehmet
Uludağ Üniversitesi/Fen-Edebiyat Fakültesi/Moleküler Biyoloji ve Genetik Bölümü.
Tepedelen, Burcu Erbaykent
AAH-6436-2021
47860936500
Keywords: Pharmacology & pharmacy
Research & experimental medicine
BPH
Cytoskeleton
EGCG
F-Actin
FAK
Paxillin
Green-tea
Epithelial-cells
Metabolic syndrome
Growth-factor
Cancer risk
Expression
Migration
Kinase
Inhibition
Apoptosis
Issue Date: 11-Oct-2017
Publisher: Elsevier
Citation: Tepedelen, B. E. vd. (2017). ''Epigallocatechin-3-gallate reduces the proliferation of benign prostatic hyperplasia cells via regulation of focal adhesions''. Life Sciences, 191, 74-81.
Abstract: Aims: Benign prostatic hyperplasia (BPH) is the most common urological disease that is characterized by the excessive growth of prostatic epithelial and stromal cells. Pharmacological therapy for BPH has limited use due to the many side effects so there is a need for new agents including natural compounds such as epigallocatechin-3-gallate (EGCG). This study was undertaken to assess the role of EGCG, suppressing the formation of BPH by reducing inflammation and oxidative stress, in cytoskeleton organization and ECM interactions via focal adhesions. Main methods: We performed MTT assay to investigate cell viability of BPH-1 cells, wound healing assay to examine cell migration, immunofluorescence assay for F-actin organization and paxillin distribution and finally immunoblotting to investigate focal adhesion protein levels in the presence and absence of EGCG. Key findings: We found that EGCG inhibits cell proliferation at the concentration of 89.12 mu M, 21.2 mu M and 2.39 mu M for 24, 48 and 72 h, respectively as well as inhibitory effects of EGCG on BPH-1 cell migration were observed in a wound healing assay. Furthermore, it was determined by immunofluorescence labeling that EGCG disrupts F-actin organization and reduces paxillin distribution. Additionally, EGCG decreases the activation of FAK (Focal Adhesion Kinase) and the levels of paxillin, RhoA (Ras homolog gene family, member A), Cdc42 (cell division cycle 42) and PAK1 (p21 protein-activated kinase 1) in a dose-dependent manner. Significance: For the first time, by this study, we found evidence that BPH-1 cell proliferation could be inhibited with EGCG through the disruption of cytoskeleton organization and ECM interactions. Consequently, EGCG might be useful in the prevention and treatment of diseases characterized by excessive cell proliferation such as BPH.
URI: https://doi.org/10.1016/j.lfs.2017.10.016
https://www.sciencedirect.com/science/article/pii/S0024320517305301
1879-0631
http://hdl.handle.net/11452/30518
ISSN: 0024-3205
Appears in Collections:Scopus
Web of Science

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